Is it important to know whether you have a spinal cord injury, a conus injury, or a cauda equina injury? The three conditions have different prognoses and therapeutic implications. A spinal cord injury interrupts the spinal tracts that go from the brain and upper spinal cord to the lower spinal cord. Lower thoracic spinal cord injuries can damage not only the spinal cord but also spinal roots that run in the spinal canal in lower thoracic and lumbosacral spinal canal. A conus injury damages the sacral segments that are present at the tip of the spinal cord and, depending on the extension of the damage, may also damage spinal roots that are present in the spinal canal near the conus. Finally, a cauda equina injury damages only the spinal roots and not the spinal cord itself. Of course, one may have combination conus and cauda equina injuries but these are relatively rare.

Injury Level

Let me first review the anatomy of the spinal cord because people are always confusing spinal cord levels with bony vertebral levels. When a surgeon talks about levels, the surgeon is usually thinking about bony (vertebral) levels. During development and childhood, the spinal column grows more than the spinal cord and is much longer than the spinal cord. As figure 1 below shows, the spinal cord levels are defined by where the spinal roots enter the spinal cord. The vertebral levels are defined by where the spinal roots exit the vertebral column. The figure was relabeled from an article that I had posted earlier.

In the cervical region, vertebral and spinal cord levels are similar. There are 8 cervical spinal cord segments and only 7 cervical vertebral segments. In the cervical spinal cord, the spinal roots exit the spinal column close to the spinal cord level. Also, in the cervical spine, the spinal roots exit just above the vertebral level. For example, C1 root exits above the C1 vertebra and the C7 root exits above the C7 vertebra. However, the C8 root exits above the T1 vertebra and the T1 root exits the spinal column above the T2 vertebra.

Spinal cord levels and vertebral levels are not the same in the thoracic and lumbosacral segments. In the lower thoracic spinal cord, the spinal cord levels are progressively further away from the vertebral levels. So, for example, the T5 cord segment is located in the T4 vertebra. The L1 cord segment is located between T8 and T9 vertebral segments. The L5 cord segment is located in the T11 vertebral segment. The sacral spinal cord (S1-S5) is located between T11 to L1. The cauda equina is located from L2 vertebra to the coccyx (the tip the spinal column).

An injury to C1 to L1 vertebral levels will damage the spinal cord. In the lower thoracic and lumbosacral spinal cord, trauma not only damages the spinal cord but also the spinal roots that exit the spinal column at the level of injury, as well as spinal roots that may be present in the spinal canal. So, for example, if you have a C5 vertebral injury, it should have damaged your C6 spinal cord and possibly the C5 spinal roots that exit the spinal column between the C4 and C5 vertebral bodies. Your neurological level should start out at C4 and may descend over time to C5 and possibly C6. If you have a T6 vertebral injury, it should have damaged your T8 spinal cord but also the T6 and T7 spinal roots that exist the spinal column above and below the T6 vertebrae.

In summary, vertebral and spinal cord levels are not the same. In the cervical spinal cord, the vertebal and spinal cord levels are similar but there are 8 cervical spinal cord segments and only 7 cervical vertebrae. In the thoracic spinal cord, the spinal cord segmental level separates from the vertebral level progressively more as one gets lower down the spinal column. The lumbosacral spinal cord is located in vertebrae T8 to L1. Spinal roots run alongside the spinal cord from T8 to L1, where the conus is located. Beyond L1, the cauda equina occupies the spinal canal.

Lower Thoracic Injury

A lower thoracic injury, i.e. T8-T12, affects the lumbar cord and upper sacral spinal cord. As shown in figure 1, the lumbar cord is situated between T8 and T11 while the S1 and S2 segment is situated at T12. An injury to the lumbar and upper sacral spinal cord will cause damage to the motoneurons that innervate the pelvic and buttock muscles (L1-L3), the upper leg muscles (L2-4), and the lower leg muscles (L4-S1). In addition, injuries at these thoracic vertebral levels will interrupt descending tracts innervating the sacral spinal cord governing sexual, bladder, and bowel function (S2-S5). The injuries may also affect the spinal roots, firstly the spinal roots that are exiting at the level of the injury and secondly the spinal roots that are descending through the spinal canal at the injury site.

A person with a T10 vertebral injury should have an injury to the L3 or L4 spinal cord, the T9 and T10 roots that exit above and below the T10 vertebra. In addition, the T10 to L4 spinal roots pass through the spinal canal at T10 may be affected. A person with a T11 vertebral injury should have an injury to the L5 spinal cord, as well as T11 and T12 spinal roots that exit the spinal cord and the spinal roots from L1 to L5 that pass through the spinal canal of the T11 vertebra. Likewise, a person with a T12 vertebral injury should have an injury to the S2 and S3 spinal segment, as well as the spinal roots of L1 to S2.

Lower thoracic injuries are therefore combinations of spinal cord and spinal root injuries. They involve both upper and motoneuronal injuries. Upper motoneuronal injuries refer to loss of motor connection between the brain and the spinal cord. Lower motoneuronal injuries refer to damage of the motoneurons themselves or the axons that connect them to the muscles. They also cause loss of ascending spinal sensory tracts as well as sensory input to the spinal cord through the spinal roots. For that reason, their neurological presentation is complex. Careful and detailed neurological examinations are required to decipher the neurological losses.

Because the thoracic cavity is strongly reinforced by the ribs, injuries to the thoracic spinal cord require massive accelerative forces and most injuries at lower thoracic levels tend to cause severe damage to the spinal cord. However, even the most severe injuries tend to spare some spinal roots passing through the canal at the injury site. So, one often sees a so-called "complete" spinal cord injury with a neurological level at L1-L5 but some sensory loss as high as T8 and involvement of abdominal muscles. In general, lower motoneuronal symptoms are restricted to the upper legs.

The classic clinical presentation of a person with lower thoracic spinal injuries is paraplegia with some preservation of proximal (hip flexors and extension) muscles, flaccid paralysis of leg muscles depending on the precise level of injury, and spastic paralysis of muscles and bladder below that level. Depending on the severity of injury, there may be sparing of sexual, bladder, and bowel function. However, even in the case of severe injuries, the persons often have spastic bladders and bowel, and spasms, indicating that the spinal cord below the injury site is still alive and kicking.

In summary, lower thoracic spinal injury usually damages a lower part of the spinal cord than indicated by the vertebral injury level. For example, a T10 vertebral injury damages the L3 and L4 spinal cord while a T12 vertebral injury damages the S2 and S3 spinal cord. The lumbosacral spinal cord is situated between T8 and L1. Injury damages not only the spinal cord but also the spinal roots that exit at the site of injury, as well as spinal roots running in the canal. Lower thoracic spinal cord injuries present with complex distributions of upper motoneuronal injuries, lower motor neuronal injuries at the site of injury, injuries to spinal roots that exit the vertebral level of injury, and damage to the spinal roots that are running in the spinal canal.

Conus Injury

A conus injury is damage to the tip of the spinal cord, involving S4/5 spinal cord segments located in the L1 vertebrae. Injury to the L1 vertebrae will also affect descending spinal roots from the L1-S3 spinal cord that exit from the L1-S5 vertebral bodies. So an L1 vertebral injury causes spinal cord gray matter damage in the S4 and S5 spinal cord segments but may also cause both motor and sensory loss due to damage to the L1-S3 spinal roots.

The first clue to the diagnosis of conus injury is evidence of damage to the L1 vertebra. Although injuries to higher vertebra such as T12 can sometimes extend down into L1 and sometimes multiple level injuries can occur, the diagnosis of a conus injury requires evidence of damage to the conus itself. This should be looked for on MRI and CT scans of the lower spinal cord at the time of injury, for any evidence of compression of the conus at L1. There may be some MRI changes of the conus that may also reveal the presence of ischemic damage (i.e. increased signal).

The second clue to the diagnosis of conus injury is the distribution of neurological deficits. These fall into three categories:
• Loss of S4 and S5 function. The S4 and S5 dermatomes are located at and around the anus. There should be loss of sensation around the anus and absent anal sphincter tone. The anal sphincter should be flaccid if the conus injury is severe. If there is partial preservation of anal and sphincter function, there may be dissociation of pinprick and touch sensations and both should be tested.
• Damage to T12 and L1 spinal roots. The T12 root exits the spinal column just above L1 vertebral body and the L1 spinal root exits just below the L1 vertebral body. Both of these roots may be affected by dislocation of the L1 vertebra. Therefore, there may be loss of sensation in the T12 dermatome situated just above the pelvic girdle and the L1 dermatome which covers most of the front of the groin and extends around the back. The T12 and L1 roots also innervate deep pelvic and hip flexion muscles and these may be affected.
• Sensory loss from injury to descending L2-S3 spinal roots. The L2 through S3 spinal roots are present in the spinal canal of the L1 vertebral body. Depending on the severity of the injury, these roots may be affected as well but these should be variable. L2, L3, L4, and L5 dermatomes cover the front of the leg while the S1 and S2 dermatomes are located in the back of the leg. Please note that the S2 and S3 dermatomes innervate the penis and scrotal area and penile sensation may be spared in a conus injury. A careful and detailed examination of sensory dermatomes should be done to identify roots that have been damaged. Please note that because these are root injuries, both touch and pinprick sensations should be affected. Sometimes in incomplete spinal cord injuries, there is sparing of pinprick while touch is absent or vice-versa; however, this should be rare when the sensory loss is due to damage to the spinal roots.
• Motor loss from injury to descending L2-S3 spinal roots. The L1 through S3 spinal roots of course innervate a great many muscles in the legs but there may be selective sparing of individual muscle groups. If the S1 root is involved, the ankle reflex should be absent. If the L3 and L4 roots are affected, the patellar (knee jerk) reflex should be absent. Severe injuries of the spinal roots may result in flaccid paralysis and atrophy of multiple leg muscles. However, there is often sparing of some muscle groups, particularly the muscles of the upper leg. Sexual and bladder function which is controlled by S2-3 may be spared or recover partly in people with conus injuries.

The third clue is the clinical presentation of a conus injury. A conus injury usually presents with sudden onset of lower back pain, bilateral motor and sensory loss, particularly anal sensation and sphincter function. Fecal incontinence is common. Patients often complain of severe low back pain and occasionally radicular pain (shooting pain from the back into the leg). If the predominant pain complaint is radicular pain, cauda equina injury should be suspected. If there is damage to the sacral spinal roots, there may be early loss of erection and the bladder may be flaccid. Knee jerks are often preserved (L3/4) but ankle jerks (S1) may be diminished. A majority will eventually recover bladder reflexes (Beric, et al., 1992)). Patients are sometimes able to walk after conus injuries.

In summary, a conus injury involves the S4/5 segment of the spinal cord situated in vertebral body L1. The injury may also involve the T12 and L1 spinal roots that exit respectfully above and below the L1 vertebral body. In addition, the spinal roots for L2 through S5 spinal roots pass through the spinal canal of the L1 vertebral body and severe occlusion of the spinal canal at L1 may result in damage to the spinal roots. The diagnosis of conus injury should include CT or MRI evidence of compression or other damage to the tip of the spinal cord at L1. Many patients may recover erection and bladder function, as well as walking, after conus injuries.

Cauda Equina Injury

The cauda equina consists of the spinal roots that descend from the spinal cord to end of the spinal column, exiting at each lumbar and sacral levels. Injury to L2 and any of the vertebral bodies below L2 may result in a cauda equina injury. The injury seldom damages all the spinal roots in the canal. The cauda equina syndrome frequently occurs as a result of disc herniation, stenosis (narrowing), or gradual dislocation of the spinal column and thus the onset of symptoms may be slow. Generally, cauda equina injury involves one side more than the other and is associated with radicular pain (shooting pain going into the affected limb). There is typically less back pain than in conus injuries.

The classic presentation of a cauda equina syndrome is saddle anesthesia, i.e. loss of sensation in the areas that innervated by the lower sacral segments (where one sits on a saddle). There is areflexic or flaccid paralysis of certain muscle groups innervated by affected spinal roots. Loss of erectile function is less common than in conus injuries (depends on whether the S2/3 roots are affected) but may happen. The bulbocavernosus reflex, penile or clitoral sensation may be absent or diminished, indicating damage to the S2/S3 roots. The cremasteric reflex (L2-L3), stroking the superior and medial part of thigh to elicit contraction of the scrotum and testes in the side of the stroked limb, should be preserved. Sensory loss should follow a dermatomal pattern. Urinary retention, if present, tends to present later or more rarely than in conus injuries.

By definition, cauda equina injury is damage to the spinal roots. The distribution of neurological loss is variable, depending of the roots involved, and motor recovery frequently occurs but sensory recovery is limited. The reason is that some motor axons can regenerate in the peripheral nerve and reinnervate muscles. If the injury is very close to the spinal cord, motor regeneration is limited. Sensory axonal regeneration and recovery is rare because sensory axons that have been interrupted cannot re-enter the spinal cord (due to the CNS-PNS barrier stops growth of axons into the spinal cord). The spinal cord itself is not damaged in cauda equina injuries.

In summary, cauda equina injuries produce saddle anesthesia, areflexic paralysis of selected lumbosacral segments, possible loss of erectile function and the bulbocavernosus reflex (S2/5) but intact cremasteric reflex (L2/3), and bowel/bladder dysfunction. Depending on the severity of injury, many people with cauda equina injuries end up with paralysis and sensory loss in certain muscle groups. Paralysis may reverse but sensory recovery is more rare. Patients often complain of radicular pain for one spinal cord segment that emanates into the affected limb. Bladder function is often affected but may be spared.

Implications for Treatment

Most of the therapeutic approaches to spinal cord injury have focused on damage to the spinal cord and regeneration of spinal tracts. People with lower thoracic spinal cord injury should benefit from such therapies. Thoracic and conus injuries would both benefit from neuronal replacement therapies. Cauda equina injuries will benefit from therapies that allow regrowth of sensory axons into the spinal cord and treatments that encourage peripheral axonal regeneration.

There are several alternative therapies that can be used to restore function in people who have spinal root damage. One is to identify those roots that are not damaged and then do nerve bridging to connect those roots with muscles and sensory nerves supplied by damaged roots. In China, for example, Dr. Shaocheng Zhang at the Second Military Hospital in Shanghai has been doing nerve rerouting in hundreds of patients. He bridges the nerves from an intact root to the distal end of a damaged root. Although not quite like a tendon transfer, it allows a patient to move muscles and feel in areas of the body.

Another approach is to stimulate regeneration in spinal roots that have been damaged. There is considerable research on methods to enhance peripheral nerve regeneration. In the case of spinal roots, there is an additional problem that must be solved: the regrowth of sensory axons into the spinal cord. Because the cell bodies of sensory axons are situated in the dorsal root ganglia just outside of the spinal cord, injury to nerve roots disrupts the sensory connections to the spinal cord. Sensory axons do not grow into the spinal cord. There are some animal studies that suggest that olfactory ensheathing glia may facilitate the entry of sensory axons into the spinal cord.

It is likely that no single therapy will work for all people with lower thoracic, conus, or cauda equina injuries. The therapies must be specifically tailored for every person, depending on which and how many spinal roots are involved, and the extent to which the spinal cord is affected by the injury. Treaments must address both upper and lower motoneuronal deficits. We must also remember that motor function requires sensory input, i.e. reflexes, proprioceptive (position sensing), and muscle feedback, essential for coordinated motor control. Thus, a solution that restores muscle innervation is not likely to restore motor control without addressing the sensory component.

Lower thoracic, conus, or cauda equina injuries often result in flaccid paralysis and muscle atrophy. Can it be reversed or prevented? Most of the atrophy that occurs is very likely to be due to non-use. In people with cervical or upper thoracic spinal cord injuries, spasticity helps maintain the muscle. However, people who have conus or cauda injuries are less spastic. There is growing evidence that intense electrical stimulation with high electrical currents can build and maintain denervated muscles. On the other hand, it may be a number of years before we will be able to replace motoneurons in the spinal cord to reinnervate muscles.

Spinal Cord Hemorrhage by Richard M. Zweifler, M.D.. Hemorrhage or bleeding of the spinal cord often happens after trauma or vascular malformations. This article from Spineuniverse.com discusses how the blood damages the spinal cord.

Tumors of the Conus and Cauda Equina by Amiram Schneiderman, Joseph T. Alexander. Tumors are a major cause of conus and cauda equina injuries. This is a review in Emedicine both the diagnosis and treatment of this condition.

Cauda Equina Syndrome by Michael S. Beeson, M.D. This review article in eMedicine was last updated on 7 April 2005. It provides a good review of the cauda equina syndrome.

Cauda equina syndrome cased by lumbar disc herniation: Commentary by John P. Kostuik. This comment in Neurosurgery Focus, Volume 16, June 2004, states that cauda equina syndrome is frequently misdiagnosed or unrecognized but can have a relatively good outcome if rapidly decompressed. Delaying surgery by more than 48 hours produces significantly worse recovery.

Cauda Equina Syndrome: Is it a Surgical Emergency? by Jason W. Nascone, William C. Lauerman, and Sam W. Wiesel of Georgetown University in 1999. This review suggests that decompression should be performed when medically feasible in patients with chronic cauda equina compression but that early decompression is important for acute cauda equina syndrome.

Wow, Wise, that is very informative. Thank you so much. I have printed it off and will send it to my daughter, Karen, as she is in this category. Three and a half years after her accident, she is back in outpatient rehab therapy again. They are so good to her at Parkwood Hospital in London, Ontario with approving her for more therapy when she needs it.

Thank you so much for all you do for people with SCI and their families. You will never know just how much you have helped so many people.

Comment

Why is it important to know since there is no treatment at this point? I am T 9 - laminectomy from T 9 to 12 - and because I have no anal sensations, loss of bladder and bowel control- I assume I am cauda equina. I have started locomotor training and FES bike and that seems to increase my muscle tone so it may help me walk without assistive device at some point. It will require a lot of work but I am eager to do it even though I will still be paraplegic. Unfortunately, I am not aware of any therapy that could help me regain my sensations and BBC, whether I am cauda equina or conus or both. Please correct me if I am wrong. The more I think about it, the more depressed I get!

gretchen 1

gretchen 1

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Great article!!!!!!! It does help one to understand a little better. Since being a T12 burst, it give me the answer as to why my bottom hurt's so bad! Look's like It feels the effect's of a broken Cauda Equnia.
Thank's
Doug

Comment

Dr Young, thanks for the great article. Not sure if you or SCI Nurse can help - but what is the best way of finding out what type of injury a person has? My surgeon told me I had a T12 burst and the VA doctors have never done a detailed examination. After reading your article I'm not sure if I have a Conus or Cauda Equina also but I would like to know. I can usually put figure things out by myself - after all I know where I have sensation and where I don't but I can't really tell whether I have a Conus or Cauda Equina.

I sort of agree with Gretchen in that since there currently isn't a cure it's not all that important. But when I was reading some of the links in your article I realized it would be nice to know my injury precisely so that I could concentrate on those parts of the articles that pertain to me. I would also say the same about future developments/research that are posted - it would help if I knew what my injury was so I could put the development in perspective.

Comment

Dr Young, thanks for the great article. Not sure if you or SCI Nurse can help - but what is the best way of finding out what type of injury a person has? My surgeon told me I had a T12 burst and the VA doctors have never done a detailed examination. After reading your article I'm not sure if I have a Conus or Cauda Equina also but I would like to know. I can usually put figure things out by myself - after all I know where I have sensation and where I don't but I can't really tell whether I have a Conus or Cauda Equina.

I sort of agree with Gretchen in that since there currently isn't a cure it's not all that important. But when I was reading some of the links in your article I realized it would be nice to know my injury precisely so that I could concentrate on those parts of the articles that pertain to me. I would also say the same about future developments/research that are posted - it would help if I knew what my injury was so I could put the development in perspective.

Thanks again.
Mike

T12 Incomplete - Walking with Crutches, Injured in Oct 2003

The diagnosis requires a meticulous neurological examination by an experienced clinician, especially for something as complicated as lower thoracic, conus, or cauda injuries. You can actually do much of it yourself, using some of the maps of the dermatomes below. If you are going to do the examination yourself, you should keep the following in mind.

1. Most of the published dermatome maps are wrong. Imagine my chagrin when I found this out in 1990, that what I thought were accurate maps were way off. But, even the ASIA dermatome map is not completely accurate. When doing your exam, remember:
• Dermatomes change after injury because sensory dermatomes expand when surrounding dermatomes are lost. For this reason, the ASIA standard recommends that the sensory testing be done at the points (the black dots) on the map. These testing points are located in parts of the dermatomes that are consistently representative of the specific dermatomes.
• If you have spinal cord injury that interrupts some spinal sensory tracts and not others, pin (spinothalamic) and touch (dorsal column) sensations may be selectively affected.

2. If you fill out the ASIA form and you have a CT/MRI scan that confirms the vertebral level of the spinal cord injury, you should be able to deduce the level of injury. So, for example,
• in your case of a T12 burst fracture, you would expect an injury to the S2/3 cord, the T11/12 roots that exit the spinal column above and below T12, and the L1 through S3 spinal roots that are present in the spinal canal at T12. The S2/3 segment innervates the penis and the bladder. So, you should not be able to feel your bladder or penis. Note that if your injury interrupts all the spinal tracts in the spinal cord at the S3/4 spinal cord, you may not have function of S4/5 and if you do, it means that you have an incomplete injury. If S4/5 segments are affected, you should have a flaccid sphincter. And so on. I would be glad to figure it out with you.

Do the dermatome map for pinprick and light touch sensation. Assess the muscle groups. In other words, fill out the form. See if you can get the radiological report for the MRI and CT scan at the time of injury. From that, you should be able to figure out the injury and level.

Wise.

[This message was edited by Wise Young on 05-17-05 at 03:01 AM.]

Comment

But the real conundrum lies in the fact that even with irreversible SCI, if therapies existed ( which we all know they don't ), the SACRAL spinal cord damage would still be irreversible. No researcher is going to take the time to work on such a difficult part of the spinal cord, when the paralysis of the patient is soo low anyways. In the land of spinal cord research, our needs haven't even been addressed yet, and we are a near bottom priority, treated as whiners to SCI doctors, when compared to someone with a higher injury. Let it be known on this day that Sacral regeneration of spinal cord tissue is not going to happen within our lifetimes, and/or 20 to 25 years. Like me, if your sexual function, bowel, and bladder have been gone for some time, then they are gone for good and nothing's gonna bring 'em back! Even Dr. Young knows deep down that this need is in the basement on the priority list, and we deserve it for having the gaul to have an injury soo low.

sherman brayton

sherman brayton

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Dr Young, thank you very much for your offer. I gladly accept it. I'll do the Asia scale tonight and post here - I really appreciate your helping me interpret the results. I do not have an MRI or CT scan from my injury but do have x-rays from my follow up visits where you can see the rods and vertbrae that the doctor rebuilt. Hopefully that will be good enough.

Brayton, as usual, what you say makes sense. We may be the last ones to be 'cured.' That's one reason I asked in another post if electrical implants - which several groups seem to be working on - are our best (soonest) hope of getting bladder control back. I wouldn't do a surgery where they had to cut any nerves but if they can develop something that will strengthen the signals from the nerves I would try it.

Comment

Okay, Dr Young, here goes. Again, thanks for your help. Now I know why you need to train people to do this - it isn't as easy as it looks. I'm glad you told me to check where the dot is on the figure - otherwise I probably would have gotten a lot wrong (it's odd that the L5 test is on the top of the foot).

On the sensory - I am a 'yes' to all of L4 and above.

L5 I couldn't feel the light touch or pin prick on my right side but could feel both on the left. The pin prick on the left didn't feel like a pin (I couldn't distinguish the pin from the Q-tip but could feel both).

S1 - no feeling.
S2 - like L5 - no feeling on right but could feel both on the left - I could distinguish the pin from the Q-tip here.
S3 - S5 - no feeling. However, when checking S3 on the left side I can feel right touch sensation on the crack of my butt right next to my anus but it doesn't look like that's where the dot is on the picture. It is relatively new (within the last few months) that I could feel here. On S4-5 I couldn't feel the pin or the Q-tip but I can feel when something larger (like a finger) is inserted. However, my anus doesn't contract even when something is inserted. In your previous post you said I shouldn't be able to feel my penis and I can't - however I can feel when I need to void. I'm not sure if that's a bladder sensation or if my stomach feels tight. If I'm awake I get very uncomfortable once my volume gets around 400 cc's and at night I wake up when I get around 600 cc's. I get erections (not like I used to) without any drugs, etc and can ejaculate.

On the motor test - I have a hard time distinguishing exactly what muscle groups works what. As far as I can tell all of the muscles on the front and inside of my legs work. My hamstrings work and my knees are strong. However, my calves are flaccid. Also, when I lay on my back I can move my legs sideways but I'm probably a 3 - very little resistance can stop that movement. When I lay on my back I can't raise my legs at all. I can't contract my butt muscles. I can move both ankles up to the neutral position but I'm probably a 3 here also - very little resistance stops any movement. My left ankle is stronger then the right but it's not very strong either - I wear 2 AFOs. I can't push down with either ankle. I can move my right big toe but can't move any toes on my left foot. Like I said, this is really sketchy - hope you can make sense of it.

I'm happy to answer any questions to clarify these comments. Thanks again.